The psychology involved with conscious breathing is interesting. For the most part we don't think about the process. It is automatic. But when one lacks O2 (or perceives that), it is both automatic--one tries to suck in air and conscious as in "Oh my God, I can't breathe." One then may do several things consciously: breathe forcefully several times and wait for the feeling of insufficiency to subside; monitor one's state alertly, for instance, no longer sleeping, or relaxing.
The one-two punch that I have experienced this past couple years has consisted of: 1. apnea, where one unconsciously stops breathing for more than 10 sec at a time (the break in the snoring), and 2. the additional insufficiency of O2 produced by restricted lungs (at 44% of normal) and pneumonia where the lungs are further compromised in re their processing of O2.
Here is how these two conditions appear to be compromising my ability to get to sleep, and once there to stay asleep, or to get back to sleep. Under normal circumstances, when I approach sleep, I slow (or automatically my body slows) my respiration rate. An outcome of this slowing is a relaxation response, felt as coming down, or indeed, going to sleep. Ordinarily this proceeds and one goes blissfully to sleep. However, a correlate of having sleep apnea, is that the slowing of respiration leads to an apnea. This, too, may pass unconsciously and any insufficiency is dealt with by the CPAP machine which is pumping air into the nostrils. (The theory is that this increased pressure of air keeps the soft palate from collapsing, which is the cause of the apnea. No air pressure, as in slow respiration, increases the likelihood of an apnea, since there is no air flow to keep the soft palate open.) And, for the 7 years that I have had the machine it has worked beautifully. I have slept like a baby and have been alert all day. Post chemo, and then post pneumonia, this has all changed.
Pavlov, in the earliest days of modern psychology, showed that any neutral stimulus could, if paired in time with a stimulus significant to the organism, acquire a similar significance as the natural one. (Does the name Pavlov ring a bell?) In his experiments where his dogs were hungry, food was the significant stimulus, and bells, tones and what not were the neutral stimuli. In a few "associations" of the neutral and biological stimulus the neutral stimulus would produce some of the same response seen to the biological one. Much later it would be shown that if the biological stimulus was a very, very powerful one, for example, the animal was sickened--as happens with food poisoning--this process did not require a precise pairing of the neutral stimulus and the biological one in time, nor did it require a number of pairings--the conditioning happened in a single trial. This is the case known to many of you as taste aversion. You get sick some time after eating a food and you avert to the taste of the food thereafter. The very thought of the food may make you queasy.
So now that first apnea, leads to a quick alerting, increased respiration rate, and indeed, some panic. This set of events has occurred more than I like to think about since I started with the pneumonia but was particularly acute whilst in PHX this winter. It has led to truly fucked up sleeping times. Jerking awake at 2 a.m. and then staying awake until after breakfast when one may (or just as likely may not) successfully get to sleep. Definite, not to be denied, urges to sleep during the day (a feature of narcolepsy). Being foiled in the subsequent attempt, until the sleep deprivation reaches such a level sleep occurs no matter. Even then, the sleep cycle that ensues may be shortened to three instead of 4 hours. Inadvertent self-treatment with alcohol helps with the first cycle, but repeated use shortens the first sleep cycle. Mike Stones' suggestion of melatonin at bedtime has also helped. In fact, I have used it successfully the last 2-3 nights and spent the full night in bed, rather than sleeping sitting up or leaving the bedroom to do computer puzzles and read the op-eds of the day.
Yesterday, a particularly acute failure to sleep mid-afternoon led me to plead with Mike for some other alternative and he said he would prescribe some tramazepan (xanax). That fell through the cracks of the system and I ended up again with the melatonin which was satisfactory. Indeed the failure to deliver on services may be good, as I don't want to be taking anything stronger.
Now we know that these sleep symptoms are also related to what is happening with my heart. The relaxation response associated with the apnea is probably also associated with the slowing of ventricular movement in the bottom chambers of the heart. Discontinuing the Tenormin (attenolol), we'll see, may decrease that slowing. Will it decrease anything else? Will it increase anything else? After 27+ years what will happen? The docs are banking on the fact that I have had little light headedness or fainting (none) during the day, so I should be able to tolerate the offset of the attenolol. We'll see.
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